Nature Communications (Mar 2019)
CRISPR-Cas9 genome editing induces megabase-scale chromosomal truncations
- Grégoire Cullot,
- Julian Boutin,
- Jérôme Toutain,
- Florence Prat,
- Perrine Pennamen,
- Caroline Rooryck,
- Martin Teichmann,
- Emilie Rousseau,
- Isabelle Lamrissi-Garcia,
- Véronique Guyonnet-Duperat,
- Alice Bibeyran,
- Magalie Lalanne,
- Valérie Prouzet-Mauléon,
- Béatrice Turcq,
- Cécile Ged,
- Jean-Marc Blouin,
- Emmanuel Richard,
- Sandrine Dabernat,
- François Moreau-Gaudry,
- Aurélie Bedel
Affiliations
- Grégoire Cullot
- Univ. Bordeaux
- Julian Boutin
- Univ. Bordeaux
- Jérôme Toutain
- Medical genetic laboratory, CHU Bordeaux
- Florence Prat
- Univ. Bordeaux
- Perrine Pennamen
- Medical genetic laboratory, CHU Bordeaux
- Caroline Rooryck
- Medical genetic laboratory, CHU Bordeaux
- Martin Teichmann
- Univ. Bordeaux
- Emilie Rousseau
- Univ. Bordeaux
- Isabelle Lamrissi-Garcia
- Univ. Bordeaux
- Véronique Guyonnet-Duperat
- INSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers
- Alice Bibeyran
- INSERM U1035, Biotherapy of genetic diseases, inflammatory disorders and cancers
- Magalie Lalanne
- Univ. Bordeaux
- Valérie Prouzet-Mauléon
- Univ. Bordeaux
- Béatrice Turcq
- Univ. Bordeaux
- Cécile Ged
- Univ. Bordeaux
- Jean-Marc Blouin
- Univ. Bordeaux
- Emmanuel Richard
- Univ. Bordeaux
- Sandrine Dabernat
- Univ. Bordeaux
- François Moreau-Gaudry
- Univ. Bordeaux
- Aurélie Bedel
- Univ. Bordeaux
- DOI
- https://doi.org/10.1038/s41467-019-09006-2
- Journal volume & issue
-
Vol. 10,
no. 1
pp. 1 – 14
Abstract
CRISPR-Cas9 has been rapidly adopted to generate cell line models of disease. Here the authors show, while attempting to establish a congenital erythropoietic porphyria model, unexpected chromosome truncations generated by a p53-dependent mechanism.
